Help with cardiac physiology

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Is anyone out there good at explaining how cardiac physiology works; particularly the depolarization/repolarization of the cells and how it correlates to phases 0-4 and what that means in the conduction process?
I've read it several times in my text and I'm also using the ECG Incredibly Easy book too but it keeps going right over my head

I'm a cardiac junkie!!!
This is VERY thorough and I find that it explains from simplex to complex.
It will familiarize/review you on cardiac terminology and basic cardiac circulation.
It will then move into the more "complex" concepts.

That page is a pretty thorough basic explanation of the conduction cycle. I would also look at the Kahn Academy stuff. That site usually has graphics and the like that shows you as you're being told what's going on... visual learning along with auditory.

In simple terms, when a cell receives a signal, it "depolarizes" meaning that it opens channels through the cell membrane that allow ions in the cell and intracellular fluid to change places. One of these ions is calcium. Normally it just hangs out outside the cell. When the cell "depolarizes" it rushes in through a channel right to the myofibrils and bind (ever so briefly) to some sites there and if there's ATP present, the myofibrils will contract. This will cause the cell to shorten. This is contraction. That cell's depolarization will be felt by it's neighbors and they too will depolarize and contract. Once the contraction is complete, the cell will pump out the calcium and the other ions that moved into the cell at the start of depolarization and pump in the ions that escaped... this is repolarization. Once the cell has finished this process, it is considered "polarized" and is at a resting potential. Now read the description I wrote with the description of what's going on at that site above and see if that kind of straightens things out for you!

Phase 0 of the action potential is the phase of rapid depolarization. During this phase the cell is stimulated and the cell membrane becomes more permeable to sodium ions. Fast sodium channels open and sodium rushes into the cell.

In phase 1, known as the period of initial repolarization, there is a brief very rapid attempt to return to resting membrane potential. During this time sodium influx ends in fast channels and potassium begins to flow out of the cell.

Phase 2 is called the plateau phase. During this phase there is an influx of calcium and sodium through the slow channels (though this sometimes also occurs during phases 0 and 1). This influx is responsible for the refractory period during which the depolarized state is maintained. Calcium also plays a role in maintenance of normal heart muscle contractility.

Phase 3 is known as the phase of rapid repolarization. Membrane potential is driven to the negative level due to the increased loss of intracellular potassium.

Phase 4, the quiescent period, is the time when the cell returns to the resting membrane potential level (-90 mV). During this period, normal distribution of sodium and potassium are restored.

The sodium potassium pump plays a role during these latter phases. ATP is required to fuel this pump and an adequate level of serum magnesium insures that the pump performs properly. Repolarization will be prolonged if the pump malfunctions, thus prolonging the QT interval on the ECG. This may lead to a potentially lethal arrhythmia, torsade de pointes, a polymorphic ventricular tachycardia.

The heart can pump unless an electrical stimulus occurs first. Generation and transmission of electrical impulses depend on the automaticity, excitability, conductivity and contractility of cardiac cells.

Automaticity refers to a cell's ability to initiate an impulse. Pacemaker cells possess this ability.

Excitability results from ion shifts across the cell membrane and indicates how well a cell responds to an electrical stimulus.

Conductivity is the ability of a cell to transmit an electrical impulse to another cardiac cell. Contractility refers to how well the cell contracts after receiving a stimulus.

As impulses are transmitted cardiac cells undergo cycles of depolarization and repolarization.

Repolarization electrical charges within the cell reverse and return to normal. The cell attempts to return to its resting state.

Cycles of depolarization-repolarization This cycle consists of 5 phases 0-4.

0 cell receives an impulse from a neighboring cell and is depolarized
1 - Early rapid repolarization (resting phase)
2 - Plateau phase period of slow repolarization
3 - Rapid repolarization phase During the last half of this phase the cell is in the relative refractory period, a very strong stimulus can depolarize it.

During phases 1,2 and the beginning of phase 3 the cell is in its absolute refractory period. No stimulus can excite the cell.
4 Resting phase of the action potential. By the end of phase 4 the cell is ready for another stimulus.

Once depolarization and repolarization occur the resulting electrical impulse travels through the heart along a pathway called the conduction system Impulses travel. SA node Located in the upper right corner of the right atrium. Pacemaker of the heart. 60-100 times a minute.

Internodal tracts and Bachmann's bundle to the AV node

Responsible for (delaying the impulses that reach it.) The nodal tissue itself has no pacemaker ability, but the tissue around it (junctional tissue) has pacemaker ability. 40-60 times a minute. This delay allows the ventricles to complete their filling phase as the atria contract. Also allows the cardiac muscle to contract to it's fullest for peak cardiac output.

Bundle of HIS: the Bundle branches Resumes the rapid conduction of the impulse through the ventricles. The bundle divides into the right and left branches. Purkenjie Fibers : Network of nervous tissue that extends through the ventricles. Can serve as a pacemaker at a rate of 20-40 times a minute.

OP, Esme has helped you with the biophysics of cell wall actions. I'm not knocking that-- I had to learn it all too, and I had to learn it more than once before it got into my thick head. But after that, I think it's more important to think about the mechanical effects of all that nifty biophysics, because that's where the rubber meets the road, so to speak. So remember that an EKG shows you the path that useful electrical impulse takes as it travels through the heart. Take a look at the diagram of the normal conduction system. That will help you visualize better.

Most muscle cells cannot contract without some sort of electrical stimulus telling them to. Cardiac muscle cells are a little different; they can generate their own little electric jolt and pass it along cell-to-cell to their neighbors IF the normal impulse doesn't come through the normal conduction pathway often enough. Remember that for later.

1)The normal impulse starts in some specialized cells in the sinoatrial (SA) node, a little patch of tissue that has the ability to do this by itself 'way up in the atria.
2) This impulse spreads thru conduction pathways in the atria, making the muscle cells contract as it goes, in a nice even pattern that empties the atria thru the tricuspid valve (right heart) and mitral valve (left heart) into the ventricles to give them something to do. That's diastole. This electricity looks like a nice round little bump, the P wave, on EKG.
3) There's a teeny pause while the impulse is gathered up in the atrioventricular (AV) node, then spreads in a nice pattern thru the ventricles, their muscle wringing like a washcloth. (The electrical signature of this action is the QRS, the big spiky deflection on the EKG.) The pressure thus developed closes the mitral and tricuspid valves but opens the pulmonic valve (right side) and aortic valve (left side) and blood gets pushed into the pulmonary artery and aorta. That's systole, and we have...a blood pressure.

If the tissue at the AV node is on strike for some reason, like it's dead after infarct (good reason), when the impulse comes down to it from the atria, it's unable to pass it along to the ventricular conduction pathway, so there is no longer a nice P wave->QRS, P->QRS, P->QRS happening. After a bit the ventricles notice that they are not getting any direction from up above. They are big and strong, but not that smart, so they only get it together to generate their own contraction slowly after one of their cells takes it upon itself to contract. Because the impulse driving them does not come down that nice dedicated pathway but has to spread cell-to-cell from there, it takes longer and doesn't look like it knows where it's going, so the QRS is wider and funny-looking.

Now if you look at the tracing for this, you see a nice regular march of P waves, indicating the atria are working they way they are supposed to, and then, at a totally different rate and not playing nice and holding hands with their friends, the ventricles tooling along on their own, slower rate. It may be fairly regular but it won't have any relationship at all to the P waves. THAT's complete heart block (3rd degree AV block).

The question is, "What's the difference between defibrillation and cardioversion?"

I liked the answer that said, "A pt with afib is alive, but the pt with vfib is dead or almost there with an ETA of five minutes."

True enough. But I think that to help you answer your own question you need to be solid on the basics of normal cardiac cycle and the conduction system that makes it happen.

1) teeny electrical impulse starts in the sinoatrial (SA) node, a little patch of tissue that has the ability to do this by itself 'way up in the atria.
2) impulse spreads thru conduction pathways in the atria, making the muscle cells contract as it goes, in a nice even pattern that empties the atria thru the tricuspid valve (right heart) and mitral valve (left heart) into the ventricles to give them something to do. That's diastole. This electricity looks like a nice round little bump, the P wave, on EKG.
3) Impulse is gathered up in the atrioventricular (AV) node, then spreads in a nice pattern thru the ventricles, their muscle wringing like a washcloth. (The electrical signature of this action is the QRS, the big spiky deflection on the EKG.) The pressure thus developed closes the mitral and tricuspid valves but opens the pulmonic valve (right side) and aortic valve (left side) and blood gets pushed into the pulmonary artery and aorta. That's systole, and we have...a blood pressure.

SO now can you see the diference between an atrial event and a ventricular one? They occur in different places. So their consequences are radically different.

Cardiac muscle is better off in terms of efficiency if it uses those organized conduction pathways to develop coordinated muscle contractions. But the conduction system can be stretched out too much, like it can be in mitral disease, because the atria have really high pressures in them (think: high-pressure systolic backflow thru the mitral valve if it doesn't close all the way OR higher pressures in the atria if the valves don't OPEN all the way when they should). Or it could lose some of its useful cells with an MI. Whatever. What happens then is that the individual cells all think they have to take over, and the atria becomes a quivering, uncoordinated mess. You no longer see a nice little round P wave, because there's no longer the nice organized flow thru the atria to make one. That's atrial fibrillation. Some people get a decrease in BP with this (this has more to do with how the ventricles behave with the varying amts of blood presented to them in "diastole", but I digress...), but blood continues to flow into the ventricles and so there is still some BP to make in systole .

VF is something else. As I mentioned above, the cardiac muscle cell has an interesting quality that no other muscle cell in the body has: it can, if conditions are right, contract on its own without an external stimulus. (To get an idea of how remarkable this is, imagine what would happen if all the muscle cells in, say, your thigh could do this without waiting for instruction from your CNS.)

Unsuccessfully treated VF is a terminal event, because a ventricle that is fibrillating is not circulating any blood out the aorta...and we all know what that means. VF on the EKG looks like a wiggly, squiggly line with small irregular points-- sorta like a very quiet EEG line. Nothing neat, nothing organized, nothing regular...because that's what the ventricle is doing: nothing neat, nothing organized, and nothing regular. All the cells are firing off in an uncoordinated fashion, and even if there are normal impulses coming thru the AV node the conduction system isn't working.

The way a defibrillator works is sorta like what happens in the old Western movie when the Sheriff finds an ugly, rowdy mob on the front porch of the jail. This is VF-- uncoordinated, unpredictable, and deadly. What does he do? He fires off his rifle, ka-BLAM! and this stops all the rabblerousing in its tracks so they can now listen to reason. Defibrillation makes all those rowdy cells discharge all at once, and while they're getting their breath back, so to speak, the normal conduction pattern can take up its work of making them orderly again. Well, we hope so, anyway. If other conditions are right (cell oxygenation, chemistries, cell wall integrity...) it will.

When you shock a fibrillating ventricle, that's called "defibrillation." When you shock a fibrillating atrium (in hopes of accomplishing the same thing: an end to chaos and a return to order) it's called "cardioversion," and has to be synchronized with the pt's own QRS (the machine does this for you, but you have to tell it to). This is because a jolt that lands in the wrong time in the ventricular conduction sequence can make for VT or VF itself, and you don't want to make extra work for yourself in this way